Tufts OpenCourseware
Author: Amelia Virostko

1. Neisseria gonorrhoeae

  1. Encounter
    1. Vaginal, anal, or oral intercourse
    2. Vertical transmission from mother to fetus
  2. Entry
    1. Use pili to attach to cervical or urethral mucosa
  3. Spread
    1. Shed into genital secretions
    2. Systemic spread in the blood leads to disseminated gonococcal infection (DGI)
    3. Males: can infect the prostate gland or epididymis
    4. Females: often infects vagina and/or rectum, occasionally spreads to cervix, uterus, and fallopian tubes resulting in pelvic inflammatory disease (PID)
  4. Damage
    1. Specifically damage ciliated cells
    2. Urethral inflammation - repeated infections can lead to urethral strictures secondary to fibrosis
    3. Prostatitis, epididymitis, or PID - can lead to infertility
    4. DGI: most common joint infection in sexually active adults
    5. Blindness in neonates
  5. Virulence Factors
    1. Pili: phase variation and antigenic variation to avoid host immune response
    2. Opa proteins: involved in adherence and invasion into host cells
    3. Lipopolysaccharide: modified to look like host substrate thereby shielding from host immune response
    4. Catalase: degrades hydrogen peroxide
    5. IgA1 protease
  6. Identification and Diagnosis
    1. Gram-negative diplococcus
    2. Can ferment glucose but not maltose
    3. Oxidase-positive facultative anaerobe
    4. Culture from urethral or cervical secretions and grow on chocolate agar
  7. Treatment
    1. Ceftriaxone IM or cipro and cefixime p.o. in a single dose
    2. Often given doxycycline to treat chlamydia since co-infection is common
  8. Outcome
    1. Males: infection often subsides in 3 weeks without treatment
    2. Females: less likely to be symptomatic therefore progression to PID or DGI is more common in women

2. Neisseria meningitides

  1. Encounter
    1. Horizontal spread through respiratory droplets
  2. Entry
    1. Inhalation
  3. Multiplication and Spread
    1. Colonize nasopharynx
    2. Rare spread to blood resulting in sepsis or meningitis
  4. Damage
    1. Spotted fever- petechiae in meningtiis indicate Neisserial origin
    2. Purpura fulminans: disseminated form causing infarcts throughout the body
    3. Chronic meningococcemia: fevers, chills, arthralgia, myalgia, petechiae
    4. Bacterial meningitis: often prior to one year of age with fever, vomiting, irritability, and lethargy
    5. Fulminant meningococcemia: septic shock producing adrenal insufficiency that can progress to DIC
  5. Virulence Factors
    1. Capsule: antiphagocytic
    2. Hemolysin
    3. Pili
    4. Opa proteins
    5. Lipopolysaccharide: blood vessel destruction and sepsis
    6. IgA1 protease
  6. Identification
    1. Same as N. gonorrhoeae except it cam ferment maltose in addition to glucose
  7. Treatment
    1. Penicillin G or ceftriaxone if suspected disseminated infection
    2. Chemoprophylaxis with rifampin or cipro
    3. Vaccine against capsule for high risk individuals
  8. Outcome
    1. Carriage: usually leads to asymptomatic colonization producing natural immunization
    2. Sepsis or meningitis: most common cause of fatal sepsis or meningitis